Summary: A new study identifies beta-frequency neural activity in the anterior cingulate cortex (ACC) as crucial for reward recognition and behavior formation. This neural signature is altered in patients with depression, suggesting that it could serve as a biomarker and potential therapeutic target for anhedonia.
This study highlights how brain activity encodes reward signals and influences future choices. These findings could lead to innovative therapies for mental health disorders involving disrupted reward processing.
Highlights:
- Beta activity in ACC: Key neural signature for recognizing rewards and shaping behavior.
- Altered by depression: Beta activity is reduced and delayed in patients with treatment-resistant depression.
- Potential biomarker: Identification of beta activity could improve the diagnosis and treatment of anhedonia.
Source: Texas Children’s Hospital
As parents, teachers, and pet owners can attest, rewards play a vital role in shaping behavior in both humans and animals. Rewards—whether in the form of treats, gifts, words of appreciation or praise, fame, or monetary benefits—act as positive reinforcement for the associated behavior.
Although this correlation between reward and future choice has been used as a well-established paradigm in neuroscience research for over a century, little is known about the neural process underlying it – how the brain encodes, remembers, and translates reward signals into desired behaviors in the future.
A recent study led by Sameer Sheth, MD, professor and vice chair for research in the Department of Neurosurgery at Baylor College of Medicine, director of the Gordon and Mary Cain Pediatric Neurology Research Foundation Laboratories, and investigator at the Jan and Dan Duncan Neurological Research Institute (Duncan NRI) at Texas Children’s Hospital, identified beta-frequency neural activity in the anterior cingulate cortex (ACC) of the frontal lobe of the brain as the key neural signature underlying processes associated with recognizing rewards and determining subsequent choices and, thus, shaping future behaviors.
In addition, the study, published in Nature Communicationsreports that this neural signature is altered in patients with depression, opening an exciting possibility of using these neural signals as a novel biomarker and a potential innovative avenue for therapy.
Anhedonia is a cardinal symptom of depression and other psychiatric disorders.
Humans derive pleasure from various physical or mental activities, sensory experiences, and interactions with family and friends.
However, people with depression often experience feelings of hopelessness, sadness, or despair for prolonged periods of time due to disengagement and anhedonia – a medical term that means the loss of the ability to feel joy or contentment in activities and things they once found enjoyable, which has a profound negative impact on their quality of life.
Anhedonia is also associated with other psychiatric and neurological disorders such as schizophrenia and bipolar disorder, substance use disorders, anxiety, and Parkinson’s disease.
Traditional antidepressants and standard treatments often fail to adequately treat this symptom in people with severe treatment-resistant depression and other conditions.
A better understanding of anhedonia may guide the development of targeted and more effective treatments for depression and related illnesses.
Reward bias response is regulated by beta activity in the frontal lobe
To identify the underlying neural basis of anhedonia, Sheth and his team recorded and analyzed neural activity from four brain regions of 15 patients with drug-resistant epilepsy who were undergoing invasive monitoring to locate the area where their seizures originated.
While their brain activity was monitored, these patients performed a perceptual discrimination task called the probabilistic reward task (PRT), a well-validated behavioral task that objectively measures anhedonia by observing subtle changes in reward-related behavior.
“We found that the unequal allocation of reward between two correct responses in this task produced a response bias in favor of the more frequently rewarded stimulus,” said lead author Dr. Jiayang Xiao, who conducted the study as a graduate student in the Sheth lab.
“We found that, based on the feedback they received, most individuals changed their subsequent responses to make choices that were likely to be rewarded, regardless of the accuracy of their responses.”
Additionally, they found that a specific signal – neuronal oscillations in the beta frequency range – originating from the anterior cingulate cortex (ACC) in the frontal lobe of the brain, showed a consistently strong and positive correlation with reward-biasing behavior and was closely related to the receipt of rewards and their value.
Additionally, they found that this specific brain region was involved in the evaluation of reward stimuli and outcomes, potentially acting as a critical node with a common reward evaluation mechanism.
“Our study answered a long-standing fundamental question in neuroscience: What specific brain region and signal regulates the classic reward-bias response, a famous example of which is Pavlovian conditioning, where dogs learned to associate the sound of a bell with food,” said co-senior author Dr. Benjamin Hayden, professor of neurosurgery at Baylor.
Reward bias response is impaired in patients with treatment-resistant depression
Next, Sheth and his team conducted a PRT study in four people with severe treatment-resistant depression. They found that reward processing in the ACC was impaired in this group. These people did not exhibit the typical behavioral response of favoring choices that are more frequently rewarded.
This observation suggests a lack of reward-biased anticipation and that their choices were less motivated by reward feedback. Consistent with this change in reward-biased behavior, beta activity in the ACC region was reduced and delayed in these individuals.
“In this study, we identified beta activity in the ACC as a potential biomarker of anhedonia,” said Sheth, also a McNair Scholar and Cullen Foundation Chair at Baylor.
“Such a biomarker could have many potential benefits, including improving the diagnosis and monitoring of symptoms in patients with severe depression and other anhedonia-related psychiatric disorders.
“Furthermore, our results present an interesting possibility that modulation of ACC beta activity could be an effective treatment for anhedonia, a hypothesis we plan to test in future clinical trials.”
Advances in neurotechnology in this research have progressed at a pace that was not previously possible, thanks in part to funding from the National Institutes of Health’s Brain Research Initiative through the Advancement of Innovative Neurotechnologies Initiative, or BRAIN Initiative.
“This study illustrates how BRAIN-funded research is already having an impact in the clinic today,” said Dr. John Ngai, director of the NIH BRAIN Initiative.
“The innovations in data collection and individualized deep brain stimulation demonstrated in this study could enable a new generation of precision treatments.”
Funding: This research reported in this press release was supported by the National Institutes of Health under grant numbers UH3 NS103549, K01 MH116364, R21 NS104953, UH3 NS100549, and R01 MH114854; and by the McNair Medical Institute of the Robert and Janice McNair Foundation.
The researchers also wish to thank the Cullen Foundation, the Jan and Dan Duncan Neurological Research Institute, and the Gordon and Mary Cain Pediatric Neurology Research Foundation Labs at Texas Children’s Hospital.
About this depression research news
Author: Rajalaxmi Natarajan
Source: Texas Children’s Hospital
Contact: Rajalaxmi Natarajan – Texas Children’s Hospital
Picture: Image credited to Neuroscience News
Original research: Free access.
“Beta activity in human anterior cingulate cortex mediates reward biases” by Sameer Sheth et al. Nature Communications
Abstract
Beta activity in the human anterior cingulate cortex mediates reward biases
The rewards we get from our choices and actions can have a major influence on our future behavior.
Understanding how behavioral reward bias is implemented in the brain is important for many reasons, including the fact that impaired reward bias is a hallmark of clinical depression.
We hypothesized that reward bias is mediated by the anterior cingulate cortex (ACC), a central cortical region associated with the integration of reward and executive control and the etiology of depression.
To test this hypothesis, we recorded neural activity during a biased judgment task in patients undergoing intracranial monitoring for epilepsy or major depressive disorder.
We found that beta oscillations (12–30 Hz) in the ACC predicted both the associated reward and the size of the choice bias, and also tracked reward receipt, thereby predicting bias on future trials.
We found a reduced magnitude of bias in depressed patients, in whom beta-specific effects were correspondingly reduced.
Our results suggest that ACC beta oscillations may orchestrate learning of reward information to guide adaptive choice and, more broadly, suggest a potential biomarker for anhedonia and indicate future development of interventions to enhance the impact of reward for therapeutic benefit.
News Source : neurosciencenews.com
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